The herpes virus is an infection that often causes painful blisters on the mouth and or genitals. Interestingly, the viral infection is common and is associated with cold sores, mononucleosis or ‘mono’, genital herpes, chickenpox, shingles, and even specific cancers. The viral infection spreads through direct skin-to-skin contact. Dependent on the type of disease the patient contracts when infected, symptoms may vary. Among these symptoms include painful sores on multiple areas of the body, itching and burning, and flu-like symptoms. Treatment includes antiviral medications to reduce symptom severity and possible outbreaks by preventing transmission. Other ways to prevent the spread of herpes includes avoiding close and intimate contact with infected individuals and using protection when engaging in sexual intercourse.
The herpes virus is commonly viewed as a deleterious infection even though most people have contracted it in their life. However, being exposed to herpes in a moderate form and early in your lifetime can have protective benefits. Previous work has indicted that herpes can help develop immune protection against severe diseases. Additionally, researchers have just published on the utility of herpes virus on treatment against cancer.
A recent article in Science Immunology, by Dr. Adam Courtney and others, indicated that the herpes virus can improve immune cell activity by promoting proteins that aid in immune cell survival. Courtney is an Assistant Professor of Pharmacology, at the University of Michigan Medical School. His work focuses on immune cell engineering to improve cancer immunotherapy. Specifically, how to activate immune cells and better direct them toward the tumor.
There are various immune cells in the body, but specific cells, known as T cells, are responsible for identifying and targeting disease. T cells are critical to improve immunotherapy, which redirect the immune response toward the tumor. Currently, work is being conducted to improve T cells by engineering them to better target and eliminate the cancer. The therapy by which patient T cells are isolated from the blood, engineered, and reinfused back into the patient is referred to as chimeric antigen receptor (CAR)-T cell therapy. This more recent form of therapy has been extremely successful in hematological malignancies. However, efficacy in solid tumors is still limited.
Courtney and his team have found a way to improve T cell function through herpes infection. Specifically, herpes infected T cells are provided with a source of proteins that help the cells survive and become activated. The team found that the viral proteins activate a series of proteins known as STAT proteins. These proteins are part of the JAK/STAT intracellular pathway which enhances T cell antitumor function. Through various laboratory techniques, researchers were able to engineer a protein from the herpes virus, which activates STAT5 in the JAK/STAT pathway, to sustain T cell function in tumors.
This groundbreaking discovery by Courtney and others improves the field’s understanding of T cell biology. Additionally, it provides an approach to improve cancer immunotherapies, including CAR-T cell therapy. CAR-T cells can be developed to enhance efficacy by activating the JAK/STAT pathway in T cells through herpes viral proteins. As a result, stronger immunotherapy can improve patient outcomes and prolong patient survival.
Article, Science Immunology, Adam Courtney, University of Michigan Medical School